Bacterqiuz2
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| Gram + rods (large)Endospores | Clostridium
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| CAT –Oxidase –Enriched media required | Clostridium
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| Strict AnaerobeMotile (except perfringes)Exotoxinstoxemia | Clostridium
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| Present in soil, alimentary tract and fecesExogenous infmalignant edema & gas gangreneEndogenous inf: dormant spores in muscle and liver | Clostridium
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| Tetanus Terminal endospores (“drumstick”) | C. tetani(neurotoxic
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| All animalsSame clinical effects of neurotoxins | C. tetani(neurotoxic
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| Lock Jaw (spasm-masticatory mm); Saw Horse stance (esp horses)/generalized muscle stiffness, altered facial expression, arched back.Tx: antitoxin(passive immunity) + toxiod + penicillin | C. tetani(neurotoxic
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| Endospores enter abrasions/ woundsinfectionToxinSynaptic inhibition =mode of actionSeverity: site of bact., amt of toxin, spp susceptibility | C. tetani(neurotoxic
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| Only killed by autoclavingBA: swarming/hemolyticFlagellar Ag’s: 10 serotypesD/D: strychnine poisoningRecovered animals not immune. | C. tetani(neurotoxic
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| Most potent biological toxin known | C. botulinum(neurotoxic
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| BotulismSubterminal endospores | C. botulinum(neurotoxic
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| Dilatd pupils, dry mmemb, decreased salivation, tongue flaccidity, dysphagia, paralysis of resp musclesabdominal breathing, paralysis neck muscles (“limberneck”), straddled stance.Fatal | C. botulinum(neurotoxic
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| Cattle, Waterfowl, HorsesSheep, mink, poultry farmed fishPigs/dogs/cats:rare/resistantPoor quality silage w/rodent carcassesoutbreaks(Ingestion of preformed toxin) | C. botulinum(neurotoxic
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| Toxininhibition of neuromuscular transmission=mode of actionTx: antiserum(neutralizes unbound toxin) | C. botulinum(neurotoxic
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| Inactivated by boiling 20min.Type C&D-most outbreaksTypes may be geographically restricted | C. botulinum(neurotoxic
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| Foals <2months(neurological dz) | “Shaker-foal Syndrome”
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| Stress on damcorticosteroids in milk | “Shaker-foal Syndrome”
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| Botulinum type B | “Shaker-foal Syndrome”
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| Vacc dam: passive transfer of neutralizing antitoxins | “Shaker-foal Syndrome”
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| “Shaker-foal Syndrome” | C. botulinum(neurotoxic
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| Blackleg | C. chauvoei(histotoxic
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| Cattle: 3months-2 years=endogenous infectionSheep: any age=exogenous infection | C. chauvoei(histotoxic
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| Gangrenous cellulites and myositis due to exotoxinsrapid death | C. chauvoei(histotoxic
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| “Braxy” (abomasitis) | C. septicum(histotoxic
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| Sheep | C. septicum(histotoxic
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| Anorexia, depression, feverrapid death | C. septicum(histotoxic
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| Winter: ingestion of frozen herbage | C. septicum(histotoxic
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| Malignant Edema | C. septicum(histotoxic
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| =cellulitis w/minimal gas gangrene | Malignant Edema
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| Tissue swelling (edema),Coldness, discoloration of overlying skin, depression, prostration (due to toxemia) | Malignant Edema
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| Rapid death w/extensive lesions | Malignant Edema
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| Gas Gangrene | C. perfringensType A(histotoxic
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| Humans/Domestic animals | C. perfringensType A(histotoxic
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| Gas productionSubcutaneous crepitation, clinical signs of toxemia (above). | C. perfringensType A(histotoxic
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| Necrotizing lethal alpha toxin (has lecithinase activityopalescence on yolk agar= Nagler Rxn) | C. perfringensType A(histotoxic
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| Anaerobic culture on BA: circular, flat, grey colonies/ double hemolysis+CAMP w/S. agalactiae | C. perfringensType A(histotoxic
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| Food poisoning | C. perfringensType A(histotoxic
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| Necrotizing enterocolitis | C. perfringensType A(histotoxic
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| Necrotic enteritis | C. perfringensType A(histotoxic
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| Canine hemorrhagic gastroenteritis | C. perfringensType A(histotoxic
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| Necrotizing enterocolitis | Pigs
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| Necrotic enteritis | Chickens
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| Canine hemorrhagic gastroenteritis | Dogs
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| Lamb dysenteryHemorrhagic enteritis | C. perfringens Type B
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| 1 week old-high mortalityCalves/Foals | C. perfringens Type B
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| (All Clostridium produce immunologically distinct exotoxins) | C. perfringens Type B
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| Sudden death: absence of microbial competition/low proteolytic activity in neonatal intestine. | C. perfringens Type B
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| “Struck”(acute enterotoxemia- specific geog. regions) | C. perfringens Type C
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| Adult Sheep+Goats, feedlot cattle, chickens, neonatal pigs | C. perfringens Type C
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| Sudden death on pasture;Gut is hemorrhagicbloody diarrhea | C. perfringens Type C
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| Pulpy Kidney Dz | C. perfringens Type D
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| Sheep | C. perfringens Type D
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| “Over-eating disease”-high grain diet/succulent pasture- worldwide. | C. perfringens Type D
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| HyperglycemiaGlycosuriaSymmetrical hemorrhagic lesions in basal ganglia and midbrain. | C. perfringens Type D
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| PM: Kidney autolysispulpy/cortical softening | C. perfringens Type D
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| Enteritis | C. perfringens Type E
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| RabbitsHemorrhagic in calves | C. perfringens Type E
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| Young rams | C. novyi Type A: “Big Head”
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| Infection of head wounds due to fighting possible rapid death | C. novyi Type A: “Big Head”
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| Necrotizing lethal alpha toxin | C. novyi Type A: “Big Head”
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| SheepCattle (+/-) | C. novyi Type Type B: “Black Disease”(Infectious necrotic hepatitis)
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| Dark skin discoloration due to SQ venus congestion | C. novyi Type Type B: “Black Disease”(Infectious necrotic hepatitis)
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| Liver damage by migrating parasitesexotoxins of C. novyihepatic necrosis | C. novyi Type Type B: “Black Disease”(Infectious necrotic hepatitis)
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| Bacillary hemoglobinuria | C.haemolyticum
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| CattleSheep (+/-) | C.haemolyticum
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| Extensive RBC destruction & liver lesions | C.haemolyticum
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| Tyzzer’s disease | C. piliformeGram –Spore forming/filamentousIntracellular pathogen
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| Foals< 6 weeksMice | C. piliformeGram –Spore forming/filamentousIntracellular pathogen
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| Severe hepatic necrosis and enteritis | C. piliformeGram –Spore forming/filamentousIntracellular pathogen
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| Chronic diarrheaHemorrhagic enterocolitis | C. difficile
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| DogsNewborn foals | C. difficile
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| Quail dzRabbits | C. colinumC. spiroforme
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